Aim: Neutrophil-lymphocyte ratio (NLR) is an easily calculated, sensitive, and accurate marker for prognosis and diagnosing sepsis, cardiovascular disease and cancer. As sepsis and septic shock are main causes of acute kidney injury (AKI) intensive care unit (ICU), we investigated whether NLR is an early predictor of AKI in patients with severe sepsis. We compared NLR's predictive power with that of other inflammation-related variables. Methods: Between December 2011 and November 2013, we enrolled 118 consecutive cases with severe sepsis admitted to ICU in this retrospective study. Levels of C-reactive protein (CRP), NLR, and white blood cell count (WBC) were recorded on admission and patients' renal function was monitored for seven consecutive days. Results: The rate of AKI occurrence 7 days after enrollment was 57.6%. NLR levels were higher in the AKI group (Group 1) than in the non-AKI group (Group 2) on the day of ICU admission (p50.001). AKI development was independently associated with NLR, Acute Physiology and Chronic Health Evaluation II (APACHE II) and duration of invasive mechanical ventilation (MV) in multivariate logistic regression analysis. The area under the receiver-operating characteristic (ROC) curve of NLR for predicting AKI was 0.986, which was superior to WBC and CRP (p50.05). The cut-off value of 10.15 for NLR had the highest validity for predicting AKI in patients with severe sepsis. The sensitivity, specificity, negative-predictive value (NPV), and positive-predictive value (PPV), for this cut-off value was 90.2%, 92.9%, 90.4%, and 92.7%, respectively. Conclusion: NLR is superior to CRP, and WBC for predicting the development of AKI in patients with severe sepsis.

Gal-3 is a promising biomarker for detecting prediabetes and diabetes.

Serum endocan concentrations were significantly elevated in women with PE versus normotensive controls, and concentrations seem to be associated with the severity of the disease.

Functional iron deficiency (FID) incidence is gradually increasing in hemodialysis (HD) patients. Recently, high levels of GDF-15 supressed the iron regulatory protein hepcidin and GDF-15 expression increased in iron-deficient patients. The relationship between FID, GDF-15, and hepcidin is currently unknown. The present study aimed to evaluate the association between GDF-15, hepcidin, and FID in chronic HD patients. Serum GDF-15 and hepcidin concentrations were measured in 105 HD patients and 40 controls. FID is defined as serum ferritin >800 ng/mL, TSAT <25 %, Hb levels <11 g/dL, and reticulocyte haemoglobin content (CHr) <29 pg. Serum GDF-15 and hepcidin levels were increased significantly in HD patients with FID, compared to HD patients without anemia and controls. GDF-15 correlated with ferritin, hepcidin, and CRP in the entire cohort. GDF-15 was related to ferritin and CRP in HD patients with FID. GDF-15 is better diagnostic marker than hepcidin for detection of FID [AUC = 0.982 (0.013) versus AUC = 0.921 (0.027); P = 0.0324]. GDF-15 appears to be a promising tool for detection of FID. High levels of ferritin and CRP correlated with GDF-15. Our results support GDF-15 as a new mediator of FID via hepcidin, chronic inflammation, or unknown pathways.

Vitamin D is mainly known for its traditional role in the bone mineralization and calcium homeostasis. Recent studies have shown that vitamin D receptors (VDR) are present in almost all the tissues and cells in the human body. In addition, several studies have revealed that vitamin D is important in immunomodulation, regulation of inflammation and cytokines, cell proliferation, cell differentiation, apoptosis, angiogenesis, muscle strength, and muscle contraction. Patients with sepsis have high mortality rate and high deficiency in vitamin D. In addition, septic patients have decreased vitamin D binding-protein (DBP) levels which further exacerbate the vitamin D deficiency. The role of vitamin D treatment in sepsis syndrome has been evaluated in animal model of sepsis where 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] administration was associated with improved blood coagulation parameters in sepsis associated with a disseminated intravascular coagulation. Vitamin D treatment in vitro has also been demonstrated to modulate levels of the systemic inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6), as well as inhibit the lipopolysaccharide (LPS)-induced activation and vasodilation of vascular endothelium. Vitamin D may enhance the induction of the antimicrobial peptides, cathelicidin and b-defensin, which have been described on mucosal and epithelial surfaces acting as the body's first line of defense against viral and bacterial pathogens. Vitamin D supplementation may divert attention from relatively simple, natural, and low-costmethods of preventing severe sepsis and septic shock. Further prospective, randomized and controlled clinical trials of adjunctive vitamin D therapy in patients who are vitamin D deficient are needed in the management of human sepsis syndrome.